Pathology, LEcture 7, Tissue Repair #1

8/8/2019 Pathology, LEcture 7, Tissue Repair #1

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Vasodilatation

Increased vascular permeability

Leukocyte recruitment and activation

Fever

Pain

Tissue damage

Prostaglandins Nitric Oxide Histamine

Histamine and serotonin C3a and C5a (by liberating vasoactive amines

from mast cells, other cells) Bradykinin

Leuktrienees C4, D4, E4 PAF Substance P

TNF, IL-1 Chemokines C3a, C5a Lukotriene B4 (Bacterial products, e.g., N-formyl methyl

peptides)

IL-1, TNF Prostaglandins

Prostaglandins Bradykinin Neuropathies

Lysosonal enzymes of leukocytes Reactive oxygen species

Nitric oxide



NM Almasri JUST

INFLAMMATORY EVENT CHEMICAL MEDIATOR

Vasodilation PGs; NO

o vascular permeability Vasoactive amines; C3a & C5a; Bradykinin;

LTC 4 , D4, & E 4; PAF

Chemotaxis,leukocyte adhesion

C5a; LTB4; bacterial products ;cytokines (IL-8)

Fever IL-1; IL-6; TNF; PGs

Pain PGs; Bradykinin

Tissue damage Lysosomal enzymes;Oxygen metabolites; NO





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University of Science & Technology is to leadmedical education using creativity and

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Restoration of tissue architectur e and functionafter an injury.

Regeneration Replacement of damaged cells by similar par enchymal cells, e.g. liver r egeneration

Requir es intact connective tissue scaffold Returns to normal state

Healing & Fibrosis (scar formation ) ECM framework is sever ely damaged Replacement by connective tissue Or ganization : in tissue spaces occupied by an

inflammatory exudates (or ganizing pneumonia)

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© 2005 Elsevier



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Remnants of the injured tissue

(attempting to restore normal structure )

Vascular endothelial cells( create new blood vessels )

Fibroblasts ( source of fibrous tissue )

Proliferations of these cells is driven by

proteins that are called GROWTHFACTORS

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Labile cells (continuously dividing & continuously dying) Stem cells divide: self r enewal and diff er entiation

Examples:

x Skin epidermis,oral cavity,vagina,cervix,ducts draining exocrine or gans.x GIT epithelium, uterus, fallopian tubes, bladder urothelium.

x Bone marrow cells

Stable cells (quiescent) Examples:

x Liver and pancr eas

x Kidney

x Smooth muscle, endothelial cells, fibroblasts

Permanent (nondividing), Examples:

x Cardiac muscle

x Neurons12



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G2

(Labile cells)G0

(Stable

cells)

(Permanent

cells)

G0

G1

S

M




© 2005 Elsevier



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Self r enewal capacity Asymmetric r eplication (after each cell division,

some progeny enter a diff er entiation pathway, while others

r emains undiff er entiated )

Capacity to develop into multiple lineagesExtensive prolif erative potential

Embryonic stem cells: Pluripotent cells that

can give rise to all tissues of the body

Adult stem cells: Restricted differentiation capacity

(lineage specific), except BM and some other adult

tissues« 16



Study of specific cell signaling and

diff er entiation steps

Production of knockout micePotentially, generation of specific cell types to

r egenerate damaged tissue (therapeutic

cloning)

Diff er entiation plasticity and transdiff er entiationhas led to the Regenerative Medicine

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Bone marrow

Liver

Skeletal muscle

Intestine

Skin

Hemetopoietic stem cells

Hering canal

Satellite cells

Base of crypts

Hair follicle bulge

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Family of proteins that control entry of the cells atspecific stages of cell cycle

Level of a specific cyclin incr eases at a specific stage,

then decr eases rapidly after the cell departs that stage In order to accomplish their function, they have to bind

to cyclin-dependent kinases (CDKs) Diff er ent combinations ar e associated with each phase

of the cell cycle They exert their function by phosphorylating certainproteins (kinase phosphorylate proteins)

Examples: Cyclin B-CDK1 activate G2 to M transition Cyclin D-CDK4,6 activate G1 to S phase

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Hypophosphorylated RB, forms a complex with E2Ftranscription factor and DP1, blocking the eff ect of E2F.

Blocking is mediated by histone deacetylase causing chromatin compaction.

CyclinD/CDK4, and cyclinE/CDK2 phosphorylate RB. Phosphorylated RB dissociated from the complex,

leading to activation of E2

F. Tar get genes for E2F include: cyclin E, DNApolymerase, thymidine kinase, dihydrofolate r eductase, and others.

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© 2005 Elsevier



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Pathology, LEcture 7, Tissue Repair #1